Background: The aim of this study was to evaluate the serum soluble CD40 ligand (sCD40L) levels, serum uroten- sin II levels, and serum leptin levels as an indirect indicator of endothelial dysfunction, inflammation, and atherosclerosis at the microvascular level, and the comparison of those values with those of the control group with a nor- mal coronary flow pattern.
Methods: The study included 35 consecutive patients (17 women, 18 men; average age: 51.20 ± 10.93 years) in our hospital who underwent coronary angiography due to objective myocardial ischemia and in whom slow coronary flow was detected. The control group included 34 consecutive patients with normal coronary flow pattern (18 women, 16 men; average age: 54.59 ± 12.40 years). The coronary flow rates of all patients and control subjects were documented by the thrombolysis in myocardial infarction (TIMI) frame count. Serum sCD40L concentrations, serum urotensin II concentrations and serum leptin concentrations were measured by an enzyme-linked immunosorbent assay method using commercially available kits.
Results: The corrected TIMI frame count for LAD, Cx, RCA, and mean TIMI frame count were significantly higher in patients with slow coronary flow (SCF), compared to subjects with normal coronary flow (43.8 ± 1.7 vs. 17.7 ± 4.7, p < 0.001; 27.9 ± 6.9 vs. 11.9 ± 4.8, p < 0.001; 25.4 ± 8.4 vs. 11.1 ± 3.1, p < 0.001; and 32.3 ± 6.4 vs. 13.7 ± 5, p < 0.001, respectively). The serum soluble CD40 ligand and serum urotensin II levels were significantly higher in the slow coronary flow group compared to the control group (12.00 ± 5.43 ng/mL--6.49 ± 5.03 ng/mL, p < 0.001; and 50.94 ± 34.28 pg/mL--26.91 ± 11.52 pg/mL, p < 0.001, respectively). In addition, there was no statistically significant difference between the slow coronary flow group and the control group with regard to serum leptin levels and hs-CRP levels (both p > 0.05).
Conclusions: This study suggests that soluble CD40 ligand and urotensin II likely play a role in the pathogenesis of slow coronary flow.